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Involvement of Subtypes γ and ε of Protein Kinase C in Colon Pain Induced by Formalin Injection
Author(s) -
Yanbo Zhang,
Kan Gong,
Weihua Zhou,
Guo Shao,
Sijie Li,
Qing Lin,
Jingjin Li
Publication year - 2011
Publication title -
neurosignals
Language(s) - English
Resource type - Journals
SCImago Journal Rank - 0.755
H-Index - 67
eISSN - 1424-8638
pISSN - 1424-862X
DOI - 10.1159/000328311
Subject(s) - protein kinase c , kinase , protein kinase a , chemistry , medicine , pharmacology , biochemistry
Protein kinase C (PKC) has been widely reported to participate in somatic pain; however, its role in visceral pain remains largely unclear. Using a colon inflammatory pain model by intracolonic injection of formalin in rats, the present study was to examine the role of PKC in visceral pain and determine which subtypes may be involved. The colon pain behavior induced by formalin injection could be enhanced by intrathecal pretreatment with a PKC activator (PMA), and alleviated by a PKC inhibitor (H-7). Wide dynamic range (WDR) neurons in the L6-S1 spinal dorsal horn that were responsive to colorectal distension were recorded extracellularly. It was found that neuronal activity was greatly increased following formalin injection. Microdialysis of PMA near the recorded neuron in the spinal dorsal horn facilitated the enhanced responsive activity induced by formalin injection, while H-7 inhibited significantly the enhanced response induced by formalin injection. Western blot analysis revealed that membrane translocation of PKC-γ and PKC-ε, but not other subtypes, in the spinal cord was obviously increased following formalin injection. Therefore, our findings suggest that PKC is actively involved in the colon pain induced by intracolonic injection of formalin. PKC-γ and PKC-ε subtypes seem to significantly contribute to this process.

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